The long-term objectives of this project are to uncover the physiological mechanisms that provide for the maintenance of an adequate venous return, and therefore an adequate cardiac filling pressure, in conditions of thermal strain in humans. Our specific aims over the next five years are as follows: 1) to devise and validate a technique that will define the role of venous outflow resistance changes in the determination of blood pooling in dependent veins during exercise and/or heat stress. 2) to determine the mechanisms that provide for the blood volume expansion known to accompany physical training. We hypothesize that these involve a decrease in cardiopulmonary baroreflex sensitivity and an increase in the capacity to synthesize plasma proteins. 3) to determine whether acute blood volume expansion will modify the peripheral vasoconstrictor response to cardiopulmonary baroreceptor unloading and thereby mimic the effects of physical training. 4) to characterize the shifts in the body fluid compartments during exercise while rehydrating with solutions of different sodium concentrations. We hypothesize that drinking dilute saline during exercise will provide a better maintenance of the body,s water balance and of blood volume as well. In order to accomplish these aims, we will study the circulatory responses of human volunteers during exercise, during gravitational stress induced by lower body negative pressure, and during progressive dehydration. We will relate the circulatory responses (e.g. change in forearm vascular resistance to the primary physiological stimuli (e.g. change in central venous pressure) in these studies. We will study these volunteers in conditions in which their blood volumes have been manipulated artificially, by serum albumin infusion, and naturally, as a result of aerobic training. We expect to learn about the physical factors that contribute to the pooling of blood in the periphery and the physiological factors that act to oppose venous pooling. These studies should improve our understanding of the control of arterial blood pressure and should provide new knowledge about the mechanisms that humans employ to resist syncope in conditions of reduced venous return.